Ion channel mutations and cancer

Figures

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  Fig. 1. Ion channels linked to cancer biology. Ion channels, including potassium (K+), sodium (Na+), calcium (Ca2+), hydrogen (H+), chloride (Cl−), and transient receptor potential (TRP) channels, play critical roles in cancer progression. Dysregulation of these channels affects key cellular processes such as proliferation, metastasis, angiogenesis, apoptosis, and metabolic adaptation.

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  Fig. 2. Ion channel-mediated signaling pathways in carcer biology. H+ channel can enhance the protons extrusion activity resulting intracellular alkalinization, which can help to maintain cancer cell metabolism. Na+ channel activity sustains Src kinase activity, which enhances actin nucleation and filament polymerization to modify cancer invasion. Ca2+ channel mediate Bcl-2-associated X protein (BAX) and calcium/calmodulin-dependent protein kinase (CAMK) signaling pathways to regulate apoptosis and proliferation in cancer development. TRP channels regulate AKT/ERK pathway. K+ channel promotes phosphorylation of MEK and thus activate ERK, which plays an important role in cancer cell's metastasis.

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  Fig. 3. Ion channel mutations in cancers. The figure summarizes channel mutations associated with cancers that were reported in recent literature. GIRK K+ channel mutations are identified in breast and adrenal cancers. Nav1.5 Na + channel mutations are associated with breast and esophageal cancers. Cav2.3 Ca2+ channel mutations are linked with lung cancer. Orai1 Ca2+ channel mutations are identified in breast cancer. Hv1 H+ channel mutations are identified in leukemia and bladder cancer. TRP channel mutations are implicated in neuroblastoma, breast, colorectal, and ovarian cancers. P2X channel mutations are associated with cervical cancer. PANX1 channel mutations are identified in breast cancer and melanoma. CLCA mutations are implicated in colorectal cancer. nAChR mutations are associated with lung cancer. NMDAR mutations are identified in melanoma.